Fade Lighting Control Method for Visual Comfort and Energy Saving

This study proposes a fade lighting control method to ensure the visual comfort of indoor occupants through gradual illuminance control while saving energy. The illuminance sensor measures the indoor illuminance and calculates the required illuminance for achieving a reference illuminance of 500 Lux. The control illuminance for each lighting is derived based on the required illuminance, and it is confirmed to fall within the threshold range of 20%. The illuminance values and time intervals for fade lighting control are calculated, ensuring that the amount of illuminance adjustment is divided by the size of the threshold range or less. In the performance evaluation, the proposed method (experimental group) was compared with the influence-based control method (control group). The result shows that this fade lighting control method minimizes the visual discomfort of occupants caused by sudden changes in lighting, and the same energy-saving of 11-42% is achieved as the control group

Acute Cerebral Infarction Following Intravenous Glycoprotein IIb/IIIa Inhibitor for Acute Myocardial Infarction

Stroke is a rare but serious complication of acute myocardial infarction (AMI). Currently, glycoprotein (GP) IIb/IIIa inhibitor is used in clinical practice for acute coronary syndromes and percutaneous coronary interventions (PCIs). The incidence of stroke in patients receiving GP IIb/IIIa inhibitor during PCIs is very low. We report the case of a 47-year-old man who presented with AMI and suffered an acute cerebral infarction after infusion of a GP IIb/IIIa inhibitor following primary PCI

Bucillamine prevents cisplatin-induced ototoxicity through induction of glutathione and antioxidant genes.

Bucillamine is used for the treatment of rheumatoid arthritis. This study investigated the protective effects of bucillamine against cisplatin-induced damage in auditory cells, the organ of Corti from postnatal rats (P2) and adult Balb/C mice. Cisplatin increases the catalytic activity of caspase-3 and caspase-8 proteases and the production of free radicals, which were significantly suppressed by pretreatment with bucillamine. Bucillamine induces the intranuclear translocation of Nrf2 and thereby increases the expression of γ-glutamylcysteine synthetase (γ-GCS) and glutathione synthetase (GSS), which further induces intracellular antioxidant glutathione (GSH), heme oxygenase 1 (HO-1) and superoxide dismutase 2 (SOD2). However, knockdown studies of HO-1 and SOD2 suggest that the protective effect of bucillamine against cisplatin is independent of the enzymatic activity of HO-1 and SOD. Furthermore, pretreatment with bucillamine protects sensory hair cells on organ of Corti explants from cisplatin-induced cytotoxicity concomitantly with inhibition of caspase-3 activation. The auditory-brainstem-evoked response of cisplatin-injected mice shows marked increases in hearing threshold shifts, which was markedly suppressed by pretreatment with bucillamine in vivo. Taken together, bucillamine protects sensory hair cells from cisplatin through a scavenging effect on itself, as well as the induction of intracellular GSH

Molecular Subgroup Analysis of Clinical Outcomes in a Phase 3 Study of Gemcitabine and Oxaliplatin with or without Erlotinib in Advanced Biliary Tract Cancer

AbstractBACKGROUND: We previously reported that the addition of erlotinib to gemcitabine and oxaliplatin (GEMOX) resulted in greater antitumor activity and might be a treatment option for patients with biliary tract cancers (BTCs). Molecular subgroup analysis of treatment outcomes in patients who had specimens available for analysis was undertaken. METHODS: Epidermal growth factor receptor (EGFR), KRAS, and PIK3CA mutations were evaluated using peptide nucleic acid–locked nucleic acid polymerase chain reaction clamp reactions. Survival and response rates (RRs) were analyzed according to the mutational status. Sixty-four patients (48.1%) were available for mutational analysis in the chemotherapy alone group and 61 (45.1%) in the chemotherapy plus erlotinib group. RESULTS: 1.6% (2/116) harbored an EGFR mutation (2 patients; exon 20), 9.6% (12/121) harbored a KRAS mutation (12 patients; exon 2), and 9.6% (12/118) harbored a PIK3CA mutation (10 patients, exon 9 and 2 patients, exon 20). The addition of erlotinib to GEMOX in patients with KRAS wild-type disease (n = 109) resulted in significant improvements in overall response compared with GEMOX alone (30.2% vs 12.5%, P = .024). In 95 patients with both wild-type KRAS and PIK3CA, there was evidence of a benefit associated with the addition of erlotinib to GEMOX with respect to RR as compared with GEMOX alone (P = .04). CONCLUSION: This study demonstrates that KRAS mutational status might be considered a predictive biomarker for the response to erlotinib in BTCs. Additionally, the mutation status of PIK3CA may be a determinant for adding erlotinib to chemotherapy in KRAS wild-type BTCs

External Ventricular Drainage before Endovascular Treatment in Patients with Aneurysmal Subarachnoid Hemorrhage in Acute Period: Its Relation to Hemorrhagic Complications

Purpose The purpose of this study was to report the authors’ experience with external ventricular drainage (EVD) before endovascular treatment (EVT) in patients with acute aneurysmal subarachnoid hemorrhage (aSAH) and to investigate its relation to hemorrhagic complications.Materials and Methods Between March 2010 and December 2017, a total of 122 patients were recruited who had an aSAH, underwent EVT to secure the ruptured aneurysm, and had EVD performed within 72 hours of rupture. The pre-embo EVD group (n=67) comprised patients who underwent EVD before EVT, and the post-embo EVD group (n=55) comprised those who underwent EVD after EVT. Results Overall, EVD-related hemorrhage occurred in 18 patients (14.8%): six (8.9%) in the pre-embo EVD group and 12 (21.8%) in the post-embo EVD group (P=0.065). No rebleeding occurred between EVD and EVT in the pre-embo EVD group. Clinical outcomes at discharge did not differ significantly between groups (P=0.384). At discharge, the final modified Rankin Scale score in patients who experienced pre-embo rebleeding was better in the pre-embo EVD group than in the post-embo EVD group (P=0.041). Current use of an antiplatelet agent or anticoagulant on admission (odds ratio [OR], 2.928; 95% confidence interval [CI], 1.234–7.439; P=0.042) and stent use (OR, 2.430; 95% CI, 1.524–7.613; P=0.047) remained independent risk factors for EVD-related hemorrhagic complications. Conclusion EVD before EVT in patients with aSAH in acute period did not increase the rate of rebleeding as well as EVD-related hemorrhagic complications. Thus, performing EVD before EVT may be beneficial by normalizing increased intracranial pressure. Especially in patients with rebleeding before the ruptured aneurysm is secured, pre-embo EVD may improve clinical outcomes at discharge